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B SEMINAR.pptx
- 1. ACID BASE BALANCE By Group 2 Students Seminar G-2 1
- 3. Objectives Definition of ACID and BASE Understand importance of maintaining acid-base balance. Understand different ways the body maintains acid base balance To diferentiat the acid-base disorders To understand the anesthetic consideration in patient with alkalosis and acidosis G-2 3
- 4. Some definitions • An acid is a molecule that releases hydrogen ions in solution • A base is a molecule that can accept a hydrogen ion • A buffer is a substance that can reversibly bind hydrogen ions and it contain weak acid and its conjugate base or weak base and its conjugate acid G-2 4
- 5. Clinical disorder We will use the suffix –osis to denote any pathological process that affect arterial PH Use the suffix –emia to denote net effect of all primary process and componsetory mechanism on arterial PH G-2 5
- 6. ACID-BASE BALANCE • Acid - Base balance is primarily concerned with two ions: – Hydrogen (H+) – Bicarbonate (HCO3 - ) G-2 6 H+ HCO3 -
- 7. ACID-BASE BALANCE Derangements of hydrogen and bicarbonate concentrations in body fluids are common in disease processes G-2 7
- 8. ACID-BASE REGULATION • Maintenance of an acceptable pH range in the extracellular fluids is accomplished by three mechanisms: – 1) Chemical Buffers • React very rapidly (less than a second) – 2) Respiratory Regulation • Reacts rapidly (seconds to minutes) – 3) Renal Regulation • Reacts slowly (minutes to hours) G-2 8
- 9. ACID-BASE REGULATION Body buffers • Chemical Buffers – The body uses pH buffers in the blood to guard against sudden changes in acidity – A pH buffer works chemically to minimize changes in the pH of a solution G-2 9 Buffer
- 10. Physiologic Buffers Oppose significant changes in pH Bicarbonate/Carbonic acid system Located primarily in RBCs H+ + HCO3 - H2CO3 H2O + CO2 Intracellular protein buffers Phosphate buffers Located within bone G-2 10
- 11. CONT……….. Their effect depends on there concentration Since H extraceluraly exchange Na and intraceluraly exchange k Acid load demenaralize the bone Alkine load increase deposition of carbonate in the bone G-2 11
- 12. Buffers extracellular carbonic acid / bicarbonate (H2CO3 / HCO3 -) haemoglobin intracellular proteins phosphoric acid / hydrogen phosphate (H3PO4 / H2PO4 - + HPO4 2-) G-2 12 Henderson-Hasselbalch equation: pH = 6.1 + log([HCO3 -] / 0.03 pCO2)
- 13. ACID-BASE REGULATION • Respiratory Regulation – When breathing is increased, the blood carbon dioxide level decreases and the blood becomes more Base – When breathing is decreased, the blood carbon dioxide level increases and the blood becomes more Acidic – By adjusting the speed and depth of breathing, the respiratory control centers and lungs are able to regulate the blood pH minute by minute G-2 13
- 14. ACID-BASE REGULATION • Kidney Regulation – Excess acid is excreted by the kidneys, largely in the form of ammonia – The kidneys have some ability to alter the amount of acid or base that is excreted, but this generally takes several days G-2 14
- 15. RENAL RESPONSE • The kidney compensates for Acid - Base imbalance within 24 hours and is responsible for long term control • The kidney in response: – To Acidosis • Retains bicarbonate ions and eliminates hydrogen ions – To Alkalosis • Eliminates bicarbonate ions and retains hydrogen ions G-2 15
- 16. HYPERKALEMIA • Hyperkalemia is generally associated with acidosis – Accompanied by a shift of H+ ions into cells and K+ ions out of the cell to maintain electrical neutrality G-2 16 H+ K+
- 17. HYPERKALEMIA Hyperkalemia is an elevated serum K+ H+ ions are buffered in cell by proteins Acidosis may cause Hyperkalemia and Hyperkalemia may cause Acidosis G-2 17 H+ K+
- 18. HYPOKALEMIA • Hypokalemia is generally associated with reciprocal exchanges of H+ and K+ in the opposite direction – Associated with alkalosis • Hypokalemia is a depressed serum K+ G-2 18 H+ K+
- 19. Maintaining Acid-Base Balance Controlled by the Lungs, Kidneys and Buffers Disrupted by Vomiting, Diarrhea, Respiratory Failure, Kidney Failure, Infections and Ingestions G-2 19
- 20. Organs involved in the regulation of A-B-balance Equilibrium with plasma High buffer capacity Haemoglobin – main buffer for CO2 Excretion of CO2 by alveolar ventilation: minimally 12,000 mmol/day Reabsorption of filtered bicarbonate: 4,000 to 5,000 mmol/day Excretion of the fixed acids (acid anion and associated H+): about 100 mmol/day
- 21. Organs involved in the regulation of A-B-balance CO2 production from complete oxidation of substrates 20% of the body’s daily production metabolism of organic acid anions such as lactate, ketones and amino acids metabolism of ammonium conversion of NH4 + to urea in the liver results in an equivalent production of H+ Production of plasma proteins esp. albumin contributing to the anion gap Bone inorganic matrix consists of hydroxyapatite crystals (Ca10(PO4)6(OH)2] bone can take up H+ in exchange for Ca2+, Na+ and K+ (ionic exchange) or release of HCO3 -, CO3 - or HPO4 2-
- 22. Principles of Acid-Base Disorders Kidneys, Lungs and Buffers maintain serum pH between 7.36 and 7.44 Blood pH is determined by the ratio of serum bicarbonate concentration ([HCO3 -]) and partial pressure of CO2 (PaCO2) G-2 22
- 23. ACIDOSIS / ALKALOSIS • An abnormality in one or more of the pH control mechanisms can cause one of two major disturbances in Acid-Base balance – Acidosis – Alkalosis G-2 23
- 24. Acid-Base Disorders Metabolic acid-base disorders and secondary metabolic compensation alter [HCO3 -] Respiratory acid-base disorders and secondary respiratory compensation alter (PaCO2) G-2 24
- 25. Acid-Base Disorders Subtle changes in pH cause large shifts in acid-base pair Determines how drugs disperse and bind and how enzymes react Proteins function within narrow spectrum of pH G-2 25
- 26. Acid-Base Disorders Acidemia: serum pH < 7.36 Alkalemia: serum pH > 7.44 Acidosis: pathologic process that lowers [HCO3 -] or raises PaCO2 Alkalosis: pathologic process that raises [HCO3 -] or lowers PaCO2 G-2 26
- 27. ACIDOSIS / ALKALOSIS • Deviations from normal Acid-Base status are divided into four general categories, depending on the source and direction of the abnormal change in H+ concentrations – Respiratory Acidosis – Respiratory Alkalosis – Metabolic Acidosis – Metabolic Alkalosis G-2 27
- 28. ACIDOSIS / ALKALOSIS • Acidosis and Alkalosis are categorized as Metabolic or Respiratory depending on their primary cause – Metabolic Acidosis and Metabolic Alkalosis • caused by an imbalance in the production and excretion of acids or bases by the kidneys – Respiratory Acidosis and Respiratory Alkalosis • caused primarily by lung or breathing disorders G-2 28
- 29. Respiratory Acidosis Decreased pH due to pulmonary CO2 retention Excess H2CO3 production leads to acidemia H+ + HCO3 - H2CO3 H2O + CO2 Acute respiratory acidosis has normal HCO3 - Chronic respiratory acidosis has elevated HCO3 - due to renal retention G-2 29
- 31. Respiratory Acidosis What are some of the causes of Respiratory Acidosis? Anything that causes your minute ventilation to decrease G-2 31
- 32. Respiratory Acidosis Airway Obstruction, aspiration Drug-induced CNS depression Alcohol, narcotics, IV sedation CNS origin Myasthenia gravis, CNS injury, Guillain- Barré Pulmonary disease Pneumonia, edema, COPD/emphysema Thoracic cage Pneumothorax, flail chest G-2 32
- 33. Respiratory Acidosis Compensation Would you expect the [HCO3 -] to increase or decrease when PaCO2 increases? G-2 33
- 34. Respiratory Acidosis Compensation Would you expect the [HCO3 -] to increase or decrease when PaCO2 increases? • H+ + HCO3 - H2CO3 H2O + CO2 G-2 34
- 35. Respiratory Acidosis Compensation • Acute – HCO3 - production from intracellular proteins – [HCO3 -] increases 1mEq/L for every 10mm Hg rise in PaCO2 • Chronic – Renal retention of HCO3 - – [HCO3 -] increases 3.5mEq/L for every 10mm Hg rise in PaCO2 – Takes 12 hours to many days for renal retention of HCO3 - – Nearly normalizes pH G-2 35
- 36. Management • Correct the minute ventilation – Establish airway – Re-expand the lung – Correct the CNS disease – Bronchodilators – Antibiotics • Chronic respiratory acidosis – Progressive decrease in sensitivity to CO2 by respiratory centers – Cautious use of oxygen, because may lose hypoxic respiratory drive and develop CO2 narcosis G-2 36
- 37. Respiratory Alkalosis Increased minute ventilation leads to decreased PaCO2 and alkalosis Acute respiratory alkalosis has normal HCO3 - Chronic respiratory alkalosis has decreased HCO3 - due to renal compensation G-2 37
- 38. Respiratory Alkalosis What causes Respiratory Alkalosis? G-2 38
- 39. Respiratory Alkalosis What causes Respiratory Alkalosis? Anything that increases your minute ventilation G-2 39
- 40. RESPIRATORY ALKALOSIS • Cause is Hyperventilation – Leads to eliminating excessive amounts of CO2 – Increased loss of CO2 from the lungs at a rate faster than it is produced – Decrease in H+ G-2 40 CO2 CO2 CO2 CO2 CO2 CO2 CO2 CO2 CO2 CO2 CO2 CO2
- 41. Respiratory Alkalosis • Hypoxia-mediated hyperventilation – High altitude, severe anemia, ventilation-perfusion mismatch • CNS mediated – Psychogenic, CVA, increased ICP (tumor/trauma) • Pharmacologic – Salicylates, caffeine, vasopressors, thyroxine • Pulmonary – Pneumonia, PE, mechanical hyperventilation, atelectasis • Hepatic – Encephalopathy G-2 41
- 42. Respiratory Alkalosis Compensation Would you expect the [HCO3 -] to increase or decrease when PaCO2 decreases? G-2 42
- 43. Respiratory Alkalosis Compensation Acute Plasma [HCO3 -] is lowered by 2mEq/L for every 10-mm Hg decrease in PaCO2 Chronic Plasma [HCO3 -] is lowered by 5mEq/L for every 10-mm Hg decrease in PaCO2 G-2 43
- 44. Metabolic Acidosis Acidemia created by increase in [H+] or decrease in [HCO3 -] Compensated for by hyperventilation to reduce PaCO2 G-2 44
- 45. Metabolic Acidosis Divided into elevated Anion Gap and normal Anion Gap AG = Na+ - (Cl- + HCO3 -) Normal = 12 +/- 3 mEq/L G-2 45
- 46. Anion Gap Metabolic Acidosis • MUDPILES – Methanol – Uremia – DKA – Propylene glycol, Paraldehyde – Infection, Iron, Isoniazid – Lactic acidosis – Ethylene glycol, Ethanol – Salicylates G-2 46
- 47. Non-Anion Gap Metabolic Acidosis GI HCO3 - loss Diarrhea, colostomy, ileostomy Renal HCO3 - loss Renal tubular acidosis Hyperparathyroidism Ingestion Acetazolamide, Calcium Chloride, Magnesium Sulfate G-2 47
- 48. Metabolic Acidosis Treatment Treat the underlying condition and the pH will gradually normalize G-2 48
- 49. Metabolic Alkalosis Alkalemia created by decrease in [H+] or increase in [HCO3 -] Compensated for by hypoventilation to increase PaCO2 G-2 49
- 50. Metabolic Alkalosis Volume-Contracted Vomiting/gastric suction Diuretics Normal Volume / Volume-Expanded Severe potassium depletion Hyperaldosteronism Cushing’s syndrome G-2 50
- 51. Metabolic Alkalosis Treatment Treat the underlying disorder Correct potassium if needed Give fluids if urine Cl- < 10mEq/L Consider acetazolamide if edematous, will increase HCO3 - secretion G-2 51
- 52. Mixed Disorders Sometimes more than one acid-base disorder is present Metabolic and respiratory processes can both be present Respiratory acidosis cannot be present with respiratory alkalosis G-2 52
- 53. ACID – BASE DISORDERS G-2 53 Clinical State Acid-Base Disorder Pulmonary Embolus Respiratory Alkalosis Cirrhosis Respiratory Alkalosis Pregnancy Respiratory Alkalosis Diuretic Use Metabolic Alkalosis Vomiting Metabolic Alkalosis Chronic Obstructive Pulmonary Disease Respiratory Acidosis Shock Metabolic Acidosis Severe Diarrhea Metabolic Acidosis Renal Failure Metabolic Acidosis Sepsis (Bloodstream Infection) Respiratory Alkalosis, Metabolic Acidosis
- 54. Anesthetic consideration related to acid-base balance anesthetic consideration in patient with acidosis -acidemia can potentiate the depressant effect of most sedative and anesthetic agents on CNS and circulatory system Increase sedation and depression of airway reflexes predispose to pulmonary aspiration Circulatory depressent effect of both volatile and IV anesthetica is also exagerated G-2 54
- 55. Halothene is the most arrythmogenic in presence of acidosis Succinylcholine should generally be avoidedin presence of acidic patients Respiratory acidosis augumented non depolarising neuromuscular blockade and may prevent its antagonism by reversal agent G-2 55
- 56. alkalosis Alkalosis increase affinity of Hgb to oxygen G-2 56
- 57. Anesthetic consideration patient with alkalemia Respiratory alkalosis prolong the duration of opoid induced respiratory depression This effect result from increased protien binding of opoid Then cerebral ischemia can occur Respiratory alkalosis mainly occur during hypoventilation G-2 57
- 58. The combination of alkalemia and hypokalemia can precipitate severe atrial and ventricular arrythmia G-2 58
- 59. Diagnosis of acid base disorder 1.examine atrial PH 2.examine Paco2 3.if arterial PH and Paco2 is not changed then look for Hco3 4.make tentative diagnosis 5.compare the change 6.if compensatory mechanism is more or less expected by definition a mixed A-B balance exist G-2 59
- 60. 7.calculate plasma anion Gap in case of metabolic acidosis 8.calculate urinary chloride concentration in case of metabolic alkalosis G-2 60
- 61. ACIDOSIS G-2 61 decreased removal of CO2 from lungs failure of kidneys to excrete acids metabolic acid production of keto acids absorption of metabolic acids from GI tract prolonged diarrhea accumulation of CO2 in blood accumulation of acid in blood excessive loss of NaHCO3 from blood metabolic acidosis deep vomiting from GI tract kidney disease (uremia) increase in plasma H+ concentration depression of nervous system accumulation of CO2 in blood accumulation of acid in blood excessive loss of NaHCO3 from blood respiratory acidosis
- 62. G-2 62 ALKALOSIS respiratory alkalosis anxiety overdose of certain drugs high altitudes prolonged vomiting ingestion of excessive alkaline drugs excess aldosterone hyperventilation loss of CO2 and H2CO2 from blood loss of acid accumulation of base metabolic alkalosis decrease in plasma H+ concentration overexcitability of nervous system hyperventilation loss of CO2 and H2CO2 from blood loss of acid accumulation of base
- 63. IN SUMMERY Four Main Acid-Base Disorders Disorder Primary Alteration Secondary Response Mechanism of Response Metabolic Acidosis in plasma HCO3 in plasma pCO2 Hyperventilation Metabolic Alkalosis in plasma HCO3 increase in pCO2 Hypoventilation Respiratory Acidosis in plasma pCO2 in plasma HCO3 Increase in acid excretion; increase in reabsorption of HCO3 Respiratory Alkalosis in plasma pCO2 in plasma HCO3 Suppression of acid excretion; decrease in reabsorption of HCO3 G-2 63
- 64. G-2 64